Insulin resistance (IR) is defined as decreased sensitivity and/or responsiveness to insulin that promote glucose disposal. A growing body of clinical and epidemiologic evidence indicates that essential hypertension and IR often coexist1. Approximately 50 percent of patients with hypertension can be considered to have IR and hyperinsulinemia1. This inextricable linkage between hypertension and IR has been identified to increase the prevalence of cardiovascular disease (CVD) and new onset of type II diabetes that is the major cause of morbidity and mortality in this clinical syndrome2. However, the driving force linking IR and hypertension remains to be fully elucidated.

In the current first-line antihypertensive agents, various drugs have been shown to have different glycometabolic effects. Diuretics or beta blockers have been proved to decrease insulin sensitivity and subsequently deteriorate IR states, whereas calcium channel blockers have been investigated to be neutral3. Only angiotensin-converting enzyme (ACE) inhibitors and angiotensin II (Ang II) type 1 (AT1) receptor antagonists have been reported to enhance insulin sensitivity and reduce new onset of type II diabetes in hypertensive individuals as highlighted in a recent meta-analysis4. Indeed, there is not even consensus as to whether or not there are pronounced benefits on IR after ARBs treatments. Bahadir et al reported that the effects of telmisartan on IR were neutral in hypertensive patients with the metabolic syndrome5. Despite intense research, drugs able to ameliorate hypertension and, at the same time, improve IR and/or hyperinsulinemia are still lacking. It is a great value to develop a new generation of antihypertensive drugs with advantages in improving metabolic disorders.

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